Spatial context in vision has profound effects on neural responses and perception. Recent animal studies suggest that the effect of surround on a central stimulus can dramatically change its character depending on the contrast of the center stimulus, but such a drastic change has not been demonstrated in the human visual cortex. To examine the dependency of the surround effect on the contrast of the center stimulus, we conducted an functional magnetic resonance imaging experiment by using a low or a high contrast in the center region while the surround contrast was sinusoidally modulated between the two contrasts. We found that the blood oxygen leveldependent response in human V1 corresponding to the center region was differentially modulated by the surround contrast, depending crucially on the center contrast: whereas a suppressive effect was observed in conditions in which the center contrast was high, a facilitative effect was seen in conditions where the center contrast was low.
When I-14C oleic acid at 120 micron Eq/hr was infused into the duodenum in normal rats in a micellar solution with mono-olein (60 mu moles/hr) in 15 mM taurocholate over 6 hr uptake was nearly complete (97%). However, when this same solution was infused into the mid small bowel in control animals uptake was incomplete (88.9 +/- 2.6%, mean +/- SEM, P < 0.01). After 4 weeks on a high fat diet, containing 45% vegetable oil by weight, oleic acid uptake increased to 98.1 +/- 0.1% (P < 0.01 compared to controls). The improved uptake of oleic acid was associated with increased dry weight of mucosa in the proximal half of the ileum from 109 +/- 8.8/20 cm in controls to 135.6 +/- 7.3 mg/20 cm in high fat diet fed rats (P < 0.05), while protein increased from 107.4 +/- 6.5 to 124.9 +/- 4.8 mg/20 cm (P < 0.05). There was no increase in DNA expressed as mg/g wet weight of mucosa or in number of cells per villus. Lipid content of the mucosa and degree of esterification of absorbed oleic also were unaltered. These results indicate that the mucosa of the proximal ileum responds to high fat feeding by hypertrophy (increased mass and protein, with no change in DNA content or cell number) and that this change is associated with more complete uptake of oleic acid reaching this part of the small bowel.
Background
Low birth weight (LBW) and fetal growth restriction are associated with the development of cardio-metabolic diseases later in life. A recent Mendelian randomization study concluded that the susceptibility of LBW infants to develop hypertension during adulthood is due to the inheritance of hypertension genes from the mother and not to an unfavorable intrauterine environment. Therein, a negative linear association has been assumed between genetically estimated maternal blood pressure (BP) and birth weight, while the observed relationship between maternal BP and birth weight is substantially different from that assumption. As many hypertension genes are likely involved in vasculature development and function, we hypothesized that BP-increasing genetic variants could affect birth weight by reducing the growth of the placenta, a highly vascular organ, without overtly elevating the maternal BP.
Methods
Using a birth cohort in the Japanese population possessing time-series fetal growth velocity data as a target and a GWAS summary statistics of BioBank Japan as a base data, we performed polygenic score (PGS) analyses for systolic BP (SBP), diastolic BP, mean arterial pressure, and pulse pressure. A causal mediation analysis was performed to assess the meditation effect of placental weight on birth weight reduced by maternal BP-increasing PGS. Maternal genetic risk score constituted of only “vasculature-related” BP single nucleotide polymorphisms (SNPs) was constructed to examine the involvement of vascular genes in the mediation effect of placental weight. We identified gestational week in which maternal SBP-increasing PGS significantly decreased fetal growth velocity.
Results
We observed that maternal SBP-increasing PGS was negatively associated with offspring birth weight. A causal mediation analysis revealed that a large proportion of the total maternal PGS effect on birth weight was mediated by placental weight. The placental mediation effect was remarkable when genetic risk score was constituted of “vasculature-related” BP SNPs. The inverse association between maternal SBP PGS and fetal growth velocity only became apparent in late gestation.
Conclusions
Our study suggests that maternal hypertension genes are strongly associated with placental growth and that fetal growth inhibition is induced through the intrauterine environment established by the placenta.
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